Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “atopy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed1981

Atopy in medical students.

Personal and immediate family histories of symptomatic atopy (asthma, eczema or allergic rhinitis) and reactivities on allergen skin prick testing were assessed in 165 medical students. Over-all, 43.0% showed a positive skin prick test to one or more allergens, 32.7% had symptomatic atopy and 55.8% had positive immediate family histories. Although the over-all incidence of skin prick test atopy is comparable with previously reported studies, the prevalence of personal and family symptomatic atopy is high in this population, especially in the female students who were significantly more likely than the males to have atopic symptoms and immediate family histories of atopic symptoms.

Asthma↗
PubMed1995

Natural history of IgE antibodies in children at risk for atopy.

BACKGROUND: The relationship between atopic diseases and high serum IgE levels has been emphasized since the mid-sixties, when IgE antibodies were discovered. A number of environmental factors, such as the type of feeding, passive smoking, viral infections, early mold, house dust mite and pet fur exposure modulate IgE synthesis and affect the development of atopic diseases. OBJECTIVE: The aim of the present study was to investigate the natural history of total and specific IgE antibodies in babies at risk for atopy, enrolled in a prospective study for the prevention of atopic disease, and follow-up from birth to 4 years of age. METHODS: One hundred seventy-four babies (90 boys and 84 girls) at risk for atopy were enrolled in this study. At the last follow-up the children had a median age of 52 months (range 43 to 74 months), dietary and environmental manipulations for the prevention of atopic diseases were recommended. All the infants were examined at the ages of 1, 3, 6, 9, and 12 months and twice each year subsequently when detailed histories were taken and signs and symptoms of atopic disease were sought. Total and specific IgE to cow milk, egg, soy, wheat, and Dermatophagoides pteronyssinus (Dpt) were measured at 6 and 12 months of life and then every year. RESULTS: During the first 24 months of life, the number of children with specific IgE to foods (n = 30) was significantly higher in comparison to the number of children with specific IgE to Dpt (n = 12) (P = .0006). Cow milk and egg were the most common offending foods. The number of children with IgE to cow milk (n = 14) was significantly higher than that with IgE to soy (n = 9) (P = .0011). Total serum IgE levels were significantly higher in the group of children who developed atopic disease in comparison with the group that did not (P < .01). CONCLUSION: Dietary and environmental measures may influence the IgE response in atopy-prone children, thus confirming the role of environmental factors in the modulation of the phenotypic expression of atopy.

Allergens↗
PubMed1996

Evidence of a strong, positive association between atopy and the HLA class II alleles DR4 and DR7.

BACKGROUND: Atopy, with or without associated asthma, provides a useful model for evaluating the genetic factors that control human immune responsiveness. HLA class II gene products are involved in the control of immune responses. OBJECTIVES: We investigated whether susceptibility or resistance to the disease was associated with HLA class II genes. METHODS: Blood samples were obtained from two groups of unrelated European-born white adults: 56 atopic patients (52 of them with asthma) and 39 healthy controls with no personal or familial history of asthma or atopy. Genomic DNA was extracted from peripheral blood lymphocytes. The exons of DQA1, DQB1, DRB and DPB1 genes were selectively amplified by the polymerase chain reaction (PCR) method. Genotyping was carried out by digestion of the amplified DNA products with allele-specific endonucleases (PCR-RFLP), which can recognize allelic variations in the polymorphic exon. RESULTS: We found no significant differences in the frequency of DPB1 alleles between patients and controls. HLA class II DR4 and DR7 alleles were present in 39.2% of the patients and in 2.5% of the healthy subjects (Pc*2 < or = 3.9 10(-3)). Conversely, DQA1*0103 and DQB1*0502 alleles were more frequent in the control subjects. These results confirm a previous study of an extended pedigree, which showed that DR4 and DR7 alleles were absent in all healthy members of the family and were frequently observed in atopic and/or in asthmatic subjects. CONCLUSION: We observed that HLA-DR 4 and DR7 alleles are significantly implicated in their susceptibility to the disease and suggest that this susceptibility is more related to atopy than to specific responses to allergens. According to previous studies, we could also submit that in atopic patients with asthma, DR4 alleles at the least, could be more closely associated with atopy than with asthma per se. Conversely, we suggest that some allelic DQA1 and DQB1 sequences might confer protection against the disease.

Adult↗
PubMedDate not supplied

[Biological and genetic basis of atopy and asthma].

Atopy is triggered by allergens and enhanced by environmental factors, but it has a clear genetic basis, as it is confirmed by the high incidence in siblings and twins. In the last few years, many authors have published genetic studies on asthmatic and atopic patients, generally with very controversial results. In the present article, IgE regulation and other immunological mechanisms which are assumed to be involved in the atopic reaction are reviewed. In the second part, the coding genes of factors, cytokines and receptors that take part in the atopy are commented, as well as review of the recent articles published about genetic markers or polymorphisms associated to these genes. The unveilling of the genetic background of atopy and asthma is a very difficult task, and it will need the definition of a specific atopic phenotype and a clear knowledge of the immunologic basis of atopy. Finally, due to racial and geographical variations a wide collaborative study of many research groups distributed all over the world will be needed.

Asthma↗
PubMed1989

Familial background of respiratory atopy. A factor of type I allergy to house dust mite in patients with atopic dermatitis.

Skin prick and radioallergosorbent tests with the house dust mite were performed in 120 patients with atopic dermatitis. The results showed that about 60% of the patients had type I allergy to the mite. Results of the prick and radioallergosorbent tests did not relate to the severity of skin involvement, nor to the seasonal fluctuation of the disease. Positive skin and radioallergosorbent tests occurred in many patients with atopic dermatitis who had a personal or family history of respiratory atopy. However, both of these tests were negative in the majority of patients with "pure" atopic dermatitis who had neither a personal nor a family history of respiratory atopy. It was suggested that a familial background of respiratory atopy is an important factor for the development of type I allergy to the house dust mite in patients with atopic dermatitis.

Adolescent↗
PubMed2002

Cow's milk protein avoidance and development of childhood wheeze in children with a family history of atopy.

BACKGROUND: In infants with a family history of atopy, food allergen avoidance has been advocated as means of preventing the development of atopic disease when breast-feeding is not possible or supplemental feeding is needed. Most infant formulas are based on cow's milk protein. Alternative choices include soya based and hydrolysed cows milk formulas. OBJECTIVES: To estimate the effect of dietary avoidance of cow's milk protein on the development of asthma or wheeze in children. SEARCH STRATEGY: The Cochrane database was searched for eligible trials until February 2002. The full text papers of all abstracts identified as RCTs were obtained and reviewed independently by two reviewers. SELECTION CRITERIA: Randomised controlled trials involving children with a family history of atopy in at least one first degree relative were considered if feeding with cow's milk based standard formula was compared to dietary avoidance of cow's milk protein using soya or other hypoallergenic formula during the initial four months of life or longer. DATA COLLECTION AND ANALYSIS: Two reviewers extracted data independently. A priori defined subgroups were the types of hypoallergenic artificial feed and dietary restrictions on mother and/or child's diet. MAIN RESULTS: Six trials used hydrolysed formula for at least 4 months in addition to dietary restrictions and in some cases dust-mite reduction measures. The risk of infants experiencing asthma or wheeze during the first year of life was reduced compared to standard cow's milk based formula (Relative Risk =0.40, 95% Confidence Intervals 0.19, 0.85). Feeding soya-based formula as opposed to standard cow's milk formula did not reduce the risk of having asthma or wheeze at any age. REVIEWER'S CONCLUSIONS: Breast-milk should remain the feed of choice for all babies. In infants with at least one first degree relative with atopy, hydrolysed formula for a minimum of 4 months combined with dietary restrictions and environment measures may reduce the risk of developing asthma or wheeze in the first year of life. There is insufficient evidence to suggest that soya-based milk formula has any benefit.

Asthma↗
PubMed1994

Evaluation of the association of acute overshift change in pulmonary function and atopy using OSHA cotton dust surveillance data.

OSHA surveillance data were collected for 769 individuals employed in four different cotton textile mills. Current workers were asked to complete a questionnaire about personal and family history of atopy or asthma. Both surveillance and survey data were available for 502 individuals. The prevalence of atopy in the population as reported by questionnaire was 18%, while asthma was reported by 4%. Dust levels at the four mills were in compliance with the cotton dust standard during the period of surveillance. No relationship was found between a self-reported history of atopy or asthma and the magnitude or frequency of acute overshift declines in forced expiratory volume during 1 second (FEV1). Nonsmokers had annual changes in FEV1 and forced vital capacity (FVC) comparable to nonexposed populations. In one of the four mills surveyed, annual declines in FEV1 and FVC for current smokers were significantly greater than declines for smokers in the other mills or the general smoking population (p < 0.02). This mill effect was also observed for subjects who were categorized as atopic (p < 0.02). For nonsmokers there appears to be no significant adverse health effect from exposure to the levels of cotton dust observed in these mills.

Adult↗
PubMed1997

Linkage analysis of bronchial hyperreactivity and atopy with chromosome 11q13.

There are two key clinical features of asthma: allergy and bronchial hyperreactivity (BHR). Some pedigree studies of atopy have indicated linkage with the high affinity IgE receptor (Fc epsilon RI-beta) gene on chromosome 11q13, but others failed to confirm this linkage. We examined the genetic linkage of three polymorphic microsatellite markers to atopy and BHR in 120 affected sibling pairs recruited from the general community. We found no linkage to atopy at any of the three 11q13 loci studied. Our findings also do not favour linkage between BHR and loci approximately 8-9 cM either side of the Fc epsilon RI-beta gene.

Adult↗
PubMed2004

Tobacco smoke exposure, wheeze, and atopy.

We investigated the effect of in utero and postnatal environmental tobacco smoke (ETS) exposure on respiratory symptoms and atopy in the first 3 years of life in children at high risk of allergic disease (both parents atopic). Three hundred and sixty-nine children were followed from birth and reviewed at ages 1 and 3 years (respiratory questionnaire, skin testing). Parental smoking questionnaires were administered, and plasma cotinine in cord and peripheral blood (at age 1 year) was measured (capillary column gas-liquid chromatography). Wheezing starting in the first year of life was significantly more common in children of smoking mothers (54.2% vs. 39.5%, P = 0.017), but not wheezing starting after age 1 year (10.8% vs. 10.9%, smoking and nonsmoking mothers, P = 0.99). Detectable cord cotinine was not associated with wheeze. More frequent wheeze in infancy was significantly more common in those with detectable 1-year cotinine (e.g., wheeze without colds, 17.8% vs. 5.6%, P = 0.02; wheeze most days, 6.5% vs. 0%, P = 0.04). ETS exposure was not associated with atopy. In the multivariate regression analysis, maternal smoking during pregnancy and/or in the first year of life remained associated with wheeze in the first year of life (odds ratio, 1.88; 95% confidence interval, 1.14-3.12; P = 0.01). ETS exposure in "high-risk" infants increases the risk of wheezing starting in the first year of life, but not after age 1 year. However, ETS exposure has little or no effect on the development of atopy. Measurement of plasma cotinine was no more useful than tobacco exposure assessment by questionnaire in our cohort.

Adult↗
PubMed2001

Linkage and allelic association of chromosome 5 cytokine cluster genetic markers with atopy and asthma associated traits.

Linkage and association of polymorphic markers in the chromosome 5q31-q33 cytokine cluster to atopy and asthma associated phenotypes have been reported by a number of groups. To investigate this region, 29 polymorphic markers were used to genotype a combined set of 233 families. These markers were ordered based upon the genetic data, supplemented by published genetic and physical maps. Significant two-point linkage was observed for asthma (most significant marker IRF1, P = 0.0002) and atopy (CD14SNP, P = 0.0001). Allelic association was observed between D5S463 and atopy (P = 0.002) and the skin prick test index (P = 0.04). The data support the possibility of three asthma/atopy loci in the 5q31-q33 region, each with a relatively small effect.

Alleles↗
PubMed1978

Atopy as a minimal immunodeficiency?

Despite impressive recent advances in the understanding of the chemical and cellular bases of the reaginic response, the pathogenesis of atopic diseases still remains a matter of speculation. The frequent finding of atopic diseases in some primary immunodeficiencies such as selective IgA deficiency and the Wiskott-Aldrich syndrome offers a unique opportunity for studying the immune mechanisms underlying the genesis of atopy. Recent studies in subjects with selective IgA deficiency have challenged the well known hypothesis that atopy is the result of defective "immune exclusion" by the secretory immune system. A number of immunological features found in the primary immunodeficiencies associated with atopic disorders suggest that defective homeostatic mechanisms regulating reaginic responses may play a major role in the pathogenesis of atopy. A thorough analysis of these disease combinations may help to generate new working hypotheses concerning the immune pathogenesis of atopic diseases.

Dysgammaglobulinemia↗
PubMed2003

Prevalence of atopy in rheumatoid arthritis in Sivas, Turkey. A prospective clinical study.

Assumed mutual antagonism of T-helper cell (Th)1 and Th2 diseases suggests that the prevalence of atopy should be decreased in rheumatoid arthritis (RA). We tried to determine that prevalence. Sixty-two patients with RA and 61 with osteoarthritis (control group) were included in the study. A questionnaire was used concerning mainly the symptoms of atopy. Skin prick tests, pulmonary function tests, chest X-rays, immunoglobulin E levels, and eosinophil counts were obtained. The prevalences of asthma, hay fever, and eczema in the RA group were 3.2%, 14.5%, and 1.6%, respectively. In the control group, they were 6.5%, 22%, and 6.5%, respectively. There was no significant difference between groups. There was also no significant difference between immunoglobulin E levels. Eosinophil counts were higher in the control group, however these values were within the normal range. Skin prick tests were obtained in seven RA patients, and eight controls revealed increased positivity. The prevalence of atopy in rheumatoid arthritis was not different from that in the general population. Our study results cannot support the concept of Th1/Th2 mutual antagonism.

Adult↗
PubMed2003

A genome-wide search for allergic response (atopy) genes in three ethnic groups: Collaborative Study on the Genetics of Asthma.

Atopy is an IgE-mediated condition known to aggregate in families and is a major risk factor for asthma. As part of the Collaborative Study on the Genetics of Asthma (CSGA), a genome-wide scan for atopy, defined by skin sensitivity to one or more common environmental allergens, was conducted in 287 CSGA families (115 African American, 138 Caucasian and 34 Hispanic). Using a nonparametric genetic analysis approach, two regions were observed in the sample of all families that yielded multipoint lod scores >1.5 (chromosome 11q, lod=1.55 between D11S1986 and D11S1998; chromosome 20p between D20S473 and D20S604, lod=1.54). Modeling that included multiple genomic positions simultaneously indicated that four chromosomal regions accounted for the majority of evidence for linkage in the combined families. These four regions are on chromosomes 10p near D10S1412 (lod=0.94), 11q near D11S1986 (lod=1.76), 17q near D17S784 (lod=0.97) and 20p near D20S473 (lod=1.74). In the subset of pedigrees giving positive evidence for linkage on chromosome 11q, the evidence for linkage increased by lod scores greater than one in four other chromosomal regions: 5q (D5S1480, lod=1.65), 8p (D8S1113, lod=1.60), 12p (D12S372, lod=1.54) and 14q (D14S749, lod=1.70). These results suggest that several regions may harbor genes contributing to the risk for atopy and these may interact with one another in a complex manner.

Adolescent↗
PubMed1998

Linkage between atopy and the IgE high-affinity receptor gene at 11q13 in atopic dermatitis families.

Atopic dermatitis is a common skin disease frequently associated with allergic disorders such as allergic rhinitis and asthma. Controversial linkage findings between atopy and markers at chromosome 11q13 led us to search chromosome 11 for genes conferring susceptibility to atopic dermatitis and atopy. Twelve families were investigated using highly polymorphic markers and a powerful model-free linkage test. Two markers gave evidence for linkage, D11S903 (P = 0.02) and FCER1B (P = 0.005). A two-point lod-score analysis between these two markers revealed significant evidence for linkage (zmax = 4.02 at (theta = 0.0). In regard to model-dependent lod-score analyses between atopic disorders and FCER1B, two-point analysis gave a lod score of z = 0.78 whereas two-locus analysis using a recessive-dominant mode of inheritance displayed a significant lod score of z = 3.55. Only 2 of 12 families showed evidence for linkage using the latter oligogenic model. In conclusion, the results of our study map the FCER1B gene in close proximity to D11S903, support the finding of Cookson et al. implicating the IgE high-affinity receptor gene (FCER1B) at 11q13, and furthermore suggest an oligogenic mode of inheritance as well as heterogeneity in the genetic susceptibility to atopy and atopic dermatitis.

Adolescent↗
PubMed1996

Infantile nephrotic syndrome and atopy.

Nephrotic syndrome presenting in the 1st year of life is often associated with a very poor prognosis for normal renal function. A small proportion of patients, particularly boys, presenting after the first 3 months of life with idiopathic-type, steroid-sensitive nephrosis, have a much better prognosis and may achieve sustained remission. We describe three boys with infantile idiopathic nephrotic syndrome of the mesangial proliferative glomerulonephritis type who went into complete remission. The patients, their first-degree relatives or both suffered from atopy (eczema, asthma or hayfever). This is the first report linking infantile nephrotic syndrome and atopy. The literature linking idiopathic nephrotic syndrome and atopy is reviewed, and the implications of our findings discussed.

Anti-Inflammatory Agents↗
PubMed2005

The environment and risk factors for atopy.

Atopy is the genetic potential to manifest the trinity of classic allergic diseases--atopic dermatitis, allergic rhinitis, and asthma. All have been observed to have increased over the past several decades. The interplay of the genetics of atopy with various environmental exposures may manifest itself in the form of allergic phenotypes or paradoxically may actually suppress the allergic response. The hygiene hypothesis offers an explanation of why certain environmental exposures early in life may suppress or activate clinical disease. Primary prevention is directed at preventing the clinical manifestations of atopy by suppressing or delaying the onset of allergic sensitivity. Studies of primary prevention have brought mixed results. Secondary prevention is directed at reducing or removing triggers in the environment of the sensitized individual. Secondary prevention measures directed at one allergen have not proven successful. Comprehensive intervention programs dealing with both allergens and other potential triggers appear beneficial.

Adolescent↗
PubMed2002

Respiratory symptoms, asthma, atopy and Chlamydia pneumoniae IgG antibodies in a general population sample of young adults.

BACKGROUND: This study was designed to test the association of Chlamydia pneumoniae infection with respiratory symptoms and atopy. METHODS: A general population sample of 369 young adults (aged 20-44 years) completed a questionnaire on respiratory symptoms and underwent skin prick testing. C. pneumoniae IgG and IgM serum titers were measured by microimmunofluorescence. Prior infection was defined by titers of IgG > or = 1:32, acute infection by titers of IgG > or = 1:512 and/or IgM > or = 1:16. RESULTS: The prevalence of cough and phlegm was higher in subjects with (19.0%) than in those without (11.4%) prior C. pneumoniae infection (p = 0.01). A similar difference was found for wheezing (14.3% vs 8.0%; p = 0.05), whereas the percentage of asthmatics was equally distributed between seropositive and seronegative subjects. IgG titers > or = 1:128 were found more frequently in atopic subjects (p = 0.04). After adjusting for any confounding factors, cough and phlegm (but not wheezing) were found significantly associated with C. pneumoniae positivity, both for 1:32 (OR 1.80; 95% CI: 1.01-3.36; p = 0.05) and for 1:128 titers (OR 2.31; 95% CI: 1.20-4.42; p = 0.01). A significant association was also found for atopy, for titers > or = 1:128 (OR 1.73; 95% CI: 1.01-3.20, p = 0.05). Acute infection was not associated with respiratory symptoms or asthma. CONCLUSION: We conclude that C. pneumoniae infection is associated with cough and phlegm and may have a role in the pathogenesis of chronic respiratory diseases. Moreover, our results indicate a relationship between atopy and C. pneumoniae infection.

Adult↗
PubMed1990

Atopy in subjects with asthma followed to the age of 28 years.

The relationship between markers of asthma and atopy was examined in 323 subjects at the age of 28 years who have been followed since the age of 7 years. Hay fever was common in all groups with severe asthma, increasing from 25% of the control group to 67% of the group with the most severe asthma, class V. Eczema was uncommon at this age in all groups. IgE levels, peripheral blood eosinophil counts, and skin reactions were significantly (p less than 0.05) higher in class V than in the control group. Increasing age was associated with a progressive fall in eosinophil counts and an increase in skin reactivity to common allergens. No change in IgE levels was observed from 21 to 28 years. A general relationship between bronchial hyperreactivity and atopic markers was found. However, only the occurrence of hay fever was significantly related to reactivity when account was taken of severity of asthma. The results indicate that the relationship between asthma and atopy observed at earlier reviews continues into adult life and that bronchial hyperreactivity and atopy are not directly linked.

Adolescent↗